Introduction to Klebsiella pneumoniae pneumonia

Contents 1 Overview 2 Disease name 3 English name 4 Alias ??of Klebsiella pneumoniae pneumonia 5 Classification 6 ICD number 7 Epidemiology 8 Causes of Klebsiella pneumoniae pneumonia 9 Pathogenesis 9.1 Susceptible groups 9.2 Source of germs 9.2.1 Hand transmission by hospital staff, home care workers and other related personnel 9.2.2 Instrument transmission 9.2.3 Pharyngeal bacterial colonization 9.2.4 Stomach bacterial colonization 9.3 Lung self-defense mechanism 9.4 Pathogenesis 9.5 Pathological changes 10 Clinical manifestations of Klebsiella pneumoniae pneumonia 10.1 Symptoms 10.2 Signs 11 Complications of Klebsiella pneumoniae pneumonia 12 Laboratory tests 12.1 Blood tests 12.2 Sputum or bronchial aspirate smears and/or culture 13 Auxiliary examination 14 Diagnosis of Klebsiella pneumoniae pneumonia 15 Differential diagnosis 16 Treatment of Klebsiella pneumoniae pneumonia 17 Prognosis 18 Prevention of Klebsiella pneumoniae pneumonia 18.1 Strict implementation of disinfection and isolation system 18.2 Gastrointestinal decontamination treatment 18.3 Protection Stomach acid barrier 18.4 Biological prevention 19 Related drugs 20 Related examinations attached: 1 Acupoints for treating Klebsiella pneumoniae pneumonia This is a redirect entry that ***shares the content of Klebsiella pneumoniae pneumonia. For the convenience of reading, Klebsiella pneumoniae pneumonia in the following text has been automatically replaced by Klebsiella pneumoniae pneumonia. You can click here to restore the original appearance, or use notes to display 1 Overview

Klebsiella pneumoniae ( Klebsiella pneumoniae, also known as Klebsiella pneumoniae or Friedlander's bacillus, is the first Gram-negative bacillus recognized to cause pneumonia. Half a century ago, gramnegative bacillary pneumonia (GNBP) was considered a very rare disease and received little clinical attention. With the exception of Klebsiella, there are few reports of pneumonia caused by gram-negative bacterium (GNB). In the past two or three decades, with the changes in susceptible populations, the widespread use of antibacterial drugs and changes in drug-resistant bacteria, and the improvement and popularization of various microbial detection technologies, GNBP has become an important disease in modern medicine in the era of antibiotics. . The proportion of GNB in ??pneumonia pathogens has increased from the original 0.5 to 5.0 to 9 to 37 in community-acquired pneumonia and more than 70 in hospital-acquired pneumonia (nosoial pneumonia, NP). To date, a large number of studies have been conducted on the clinical and epidemiological characteristics, susceptibility factors, etiological diagnosis, anti-infective treatment drugs and methods of GNBP acquired in and outside the hospital, but the mortality rate remains high. Studying and summarizing the pathogenesis and diagnosis and treatment experience of GNBP will still be an important topic in the field of pulmonary infectious diseases in the future.

There are dozens of aerobic and facultative anaerobic GNBs reported in the literature that can cause pneumonia, but the most common clinical ones are K. pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa, and Acinetobacter , Escherichia coli, Proteus and Legionella and several other species. Meta-analysis shows that the overall incidence of nosocomial pneumonia in my country is 2.33, and K. pneumoniae accounts for 10.1 of all nosocomial pneumonia pathogens.

Although there are many prospective and retrospective surveys, the exact incidence of pneumonia caused by B. pneumoniae in the social population is difficult to estimate. In recent years, the clinical isolation rate of B. pneumoniae has been on a downward trend.

Klebsiella pneumoniae pneumonia has a sudden onset and is characterized by chills, high fever, cough, purulent sputum, and brick-red jelly sputum. 80% of patients have chest pain, which is mainly caused by inflammation that invades the parietal pleura. Some patients have gastrointestinal symptoms, such as nausea, vomiting, diarrhea, jaundice, etc. The whole body is weak, and some patients have symptoms of upper respiratory tract infection. A very small number of patients present with a chronic disease course, which may also be delayed from an acute disease course. Symptoms include low-grade fever, cough, and weight loss. Signs include acute illness, dyspnea, and cyanosis. A few patients may develop jaundice and shock. People with positive blood cultures generally have a poor prognosis. Due to the high drug resistance rate of pneumonia bacteria, the case fatality rate is 20 to 30. Treatment of K. pneumoniae pneumonia includes anti-infective therapy and supportive care. Whether anti-infective treatment is effective or not directly affects the prognosis of the disease. 2 Disease name

Klebsiella pneumoniae 3 English name

Klebsiella pneumoniae

4 Alias ??of Klebsiella pneumoniae

Friedlander's pneumonia; Klebsiellar pneumonia; Klebsiella pneumonia; Klebsiella pneumonia; Klebsiella pneumonia; Klebsiella pneumonia; Klebsiella pneumonia 5 categories

Respiratory medicine gt; Infectious diseases gt; Bacterial pneumonia 6 ICD number

J15.0 7 Epidemiology

The incidence rate of Klebsiella pneumoniae pneumonia in domestic and foreign statistics There are certain differences. In China, there are mainly surveys conducted in several large hospitals and local areas, and they focus on nosocomial pneumonia. According to statistics from Peking Union Medical College Hospital from 1983 to 1992, the incidence rate of Klebsiella pneumoniae pneumonia was 40.9, ranking second among NPs. According to worldwide statistics, Klebsiella pneumoniae pneumonia accounts for 1 to 8% of all pneumonia. The incidence rate in the United States in the early 1980s was 7.4. Among them, the proportion of nosocomial pneumonia was 12.8 in the early 1980s, and 12.8 in the middle and late 1980s. 11.6 (NNIS Report). Second only to Pseudomonas aeruginosa and Staphylococcus aureus pneumonia, it ranks third in NP. The actual investigation of community-acquired pneumonia (CAP) is limited by many factors and lacks unified reporting. Klebsiella pneumoniae pneumonia accounts for 16 to 64% of the incidence of gram-negative bacilli pneumonia in CAP, and Klebsiella pneumoniae is now considered to be one of the common pathogenic bacteria of CAP. In the 1990s, foreign statistics showed that the incidence rate of Klebsiella pneumoniae pneumonia was 7. Although it dropped slightly and the ranking dropped to 4th, the actual number of cases was basically the same as in the 1980s, and the so-called " The number of "superinfections" has increased significantly.

In recent years, surveys of NP have found that mixed infections between Klebsiella pneumoniae and other bacteria and fungi have gradually increased. According to a 1989 statistics, among 95 patients with Candida albicans respiratory tract infection , the number of patients with Klebsiella pneumoniae infection was around 38.9. In addition, various studies have found that the incidence of bacteremia in patients with Klebsiella pneumoniae pneumonia is around 25, and the pathogenic bacteria can often be determined clinically through blood culture.

Before the application of antibiotics, the mortality rate of Klebsiella pneumoniae pneumonia was as high as 51 to 97. With the application of various antibiotics and the adoption of preventive measures, the mortality rate has been greatly reduced. However, compared with other types of pneumonia, the case fatality rate is still high. According to statistics from the US NNIS, the case fatality rate of nosocomial Klebsiella pneumonia was 18 to 30 in the late 1960s to the late 1980s. According to domestic statistics from Peking Union Medical College Hospital, the fatality rate of nosocomial Klebsiella pneumonia was 18 to 30. The fatality rate of Burmese burgdorferi pneumonia is 50%.

8 Causes of Klebsiella pneumoniae pneumonia

Klebsiella pneumoniae is Gram-negative, inactive, capsuled, in pairs or short chains, and grows easily on ordinary culture media. The colonies on solid media are higher than the surface and are characterized by being smooth and sticky. According to different capsular antigen components, pneumoniae bacteria can be divided into 75 subtypes. Types 1 to 6 are mainly responsible for causing pneumonia. They can quickly adapt to the host environment and survive for a long time, and are prone to develop resistance to various antibiotics. pneumoniae pneumonia is more common in middle-aged and elderly people. Any situation that causes the body's immune function to be compromised can become a cause of infection. For example, the use of hormones and immunosuppressive drugs, as well as anti-metabolite drugs, causes systemic immune dysfunction and various serious diseases (such as tumors, diabetes, chronic liver disease, leukopenia, leukemia, etc.); certain invasive examinations, traumatic treatments and surgeries , using contaminated respirators, nebulizers, etc. may lead to infection. Hand transmission of hospital staff, patients and chronic germ carriers are all sources of germs. 9 Pathogenesis 9.1 Susceptible groups

Klebsiella pneumoniae pneumonia is an opportunistic infectious disease. Its occurrence and development depend on certain pathological foundations. Common susceptibility factors include:

(1) Patients with chronic diseases: Common ones include long-term alcoholism, diabetes, chronic heart and lung diseases, cancer and leukopenia patients, etc.

(2) Those who take long-term treatment with a variety of antibiotics, glucocorticoids, immunosuppressive drugs and cytotoxic drugs.

(3) Patients who have been treated in the intensive care unit (ICU) for a long time, including post-surgical monitoring patients and patients with advanced neuromuscular diseases.

(4) Patients using respiratory therapy devices. Such as the application of mechanical ventilation, atomization treatment, etc. NP in this type of patients has been the focus of attention from all aspects in recent years, and its morbidity and mortality rates are much higher than the average levels of Klebsiella pneumoniae pneumonia. 9.2 Sources of germs

The main sources of germs are patients and chronic germ carriers (such as chronic alcoholics). The spread of germs mainly occurs through the following ways: 9.2.1 (1) Hospital staff, Hand transmission among family caregivers and other related personnel

The main reason for hand transmission is the failure to strictly implement disinfection and cross-infection prevention measures. 9.2.2 (2) Device transmission

Common device transmission includes nebulizers, ventilators and their pipelines, endotracheal intubations, nasogastric tubes, etc. ① Nebulizer: It is a common source of infection. In addition to causing cross-infection, it can also cause environmental pollution. According to Merlz's report, the fulminant Klebsiella pneumoniae pneumonia that occurred in Bilevui Hospital was caused by nebulizer contamination. ② Ventilator: During the mechanical ventilation process, because the pipeline is connected to the patient's respiratory tract to form a closed cycle, coupled with factors such as environmental pollution, lax disinfection, and untimely tube replacement, the colonization rate of bacterial colonies in the pipeline is very high. At the same time, due to the gas Compression and the temperature difference between the pipeline and the surrounding environment cause water vapor to condense in the pipeline (especially where the trachea and intubation are connected). According to reports, the amount of water vapor condensation in ordinary unheated pipelines reaches 20 to 40ml per hour, which is the main place for bacteria to survive. According to reports, the water in the pipeline near the intubation site contains more than 200,000 bacteria per milliliter. Turning the patient's vagina, etc. will cause the bacteria-containing water to flow directly into the lower respiratory tract. At present, there are few independent heating pipelines, which are expensive and cumbersome to maintain. It is difficult to solve them immediately. According to the requirements of the U.S. Centers for Disease Control (CDC), tubes should be replaced every 24 hours. However, clinical practice has found that there is no difference in the number of bacteria between tube replacement and tube replacement every 48 hours. Some literature even states that tube replacement should be done every 24 hours. The incidence of road pneumonia is higher. The specific clinical requirements will depend on the monitoring results and actual conditions. According to relevant literature reports, the incidence of pneumonia in patients who receive mechanical ventilation is 7 to 21 times that of those who do not receive mechanical ventilation, among which Klebsiella pneumoniae is one of the most common pathogenic bacteria. ③Tracheal intubation: Tracheal intubation is a device with dense colonies. According to an electron microscope examination, colonies can be seen in 95% of the area of ????the intubation, 86% of which are completely covered by colonies. The reasons are: A. Intubation damages the pharynx and destroys the The host's natural defense mechanism.

B. Destroys the cleaning function of airway cilia. C. Destruction of swallowing reflex and activity. D. The intubation tube cannot be replaced frequently, and internal and external infections are mixed during sputum suction. In view of the above reasons, the endotracheal intubation directly crosses the pharyngeal barrier, and the leakage of secretions around the cuff allows bacteria to directly enter the lower respiratory tract. 9.2.3 (3) Pharyngeal colony colonization

The pharynx is the most common colonization site for Klebsiella pneumoniae and is also the direct source of the bacteria for pneumonia. The detection rate of Klebsiella pneumoniae in the pharynx of normal people is less than 1, while the detection rate of Gram-negative bacilli in severe patients is as high as 70 after repeated pharyngeal secretion cultures. According to a study report, among 26 patients with nosocomial Klebsiella pneumoniae pneumonia in an ICU, 22 (84) patients had Klebsiella pneumoniae detected in the pharynx beforehand. The bacterial colonization of the pharynx is closely related to the adsorption capacity of the pharyngeal epithelial cells. On the surface of pharyngeal epithelial cells, there are corresponding bacterial adsorption receptors. Under normal circumstances, these receptors are covered by pharyngeal fibronectin (Fibronectin), but under pathological conditions (alcohol abuse, nutritional imbalance, smoking, broad-spectrum application Antibiotics and endotracheal intubation, etc.), various non-specific proteases are released into the oral cavity. They can digest the fibrin on the surface of epithelial cells. At this time, the receptors are exposed, and the bacteria will "chain-like" adsorption to them.

Klebsiella pneumoniae has a very high affinity for pharyngeal epithelial cells. But the strange thing is that it does not have a brush edge for adsorption, so its adsorption principle is still unclear. The survival period of Klebsiella pneumoniae in the oropharynx can often reach several months, which is especially obvious in patients with chronic alcoholism. According to statistics, about 29% of chronic alcoholics are carriers of Klebsiella pneumoniae in the pharynx. According to a follow-up survey of pharyngeal bacteria in patients discharged from pneumonia after recovery, it was found that the pharyngeal colonies of patients over 75 years old disappeared 4 weeks after discharge (including Pseudomonas aeruginosa, Staphylococcus aureus, etc.), but Klebsiella pneumoniae Most of them persisted, and by the end of the investigation, there were still 43 Klebsiella pneumoniae colonies that had not disappeared.

The factors that affect the colonization of Klebsiella pneumoniae colonies in the pharynx are: ① Changes in host cells: Various receptors on the host epithelial cells receive corresponding bacteria, and the application of cyclosporine A can inhibit the receptors. The body's adsorption capacity for Klebsiella pneumoniae. ② Changes in bacteria: This includes whether the bacteria themselves have a capsule, the type of surface adsorbates and the characteristics of release by external contact, etc. The surface adsorbates of Klebsiella pneumoniae are still unknown. ③ Changes in the local microenvironment: The pH value in the environment has the greatest impact. When the pH is 6.5 to 7.2, the adsorption capacity of bacteria can dramatically increase to the highest level. In addition, the concentration of mucin and protease in sputum and oropharyngeal secretions The increase in IgA level and the decrease in IgA level can both enhance the adsorption capacity. Improper application of antibiotics can eliminate the inhibitory flora of gram-negative bacilli in the pharynx (such as Streptococcus) and increase their colonization and growth. 9.2.4 (4) Colony colonization of stomach

Normal human stomach remains sterile due to acid barrier and other functions. Research in the past ten years has shown that changes in the gastric environment can also cause colonization of bacterial colonies, which has become an important bacterial source for pharyngeal transplantation of intestinal resident bacteria such as Klebsiella pneumoniae. Pathological conditions that cause an increase in gastric flora include: ① Older age and reduced functions of the stomach itself. ② Achlorhydria and loss of acid barrier. ③ Various acute and chronic gastrointestinal diseases. ④ Nutritional imbalance. ⑤Use antacids and/or H2 receptor antagonists. When gastric acid deficiency or pH value increases, the number of gastric bacteria can be as high as 1 million to 100 million per milliliter. Coupled with abnormal reflexes, the gastric bacterial colonies will reflux to the pharynx, forming pathogenic bacteria of pneumonia and bronchitis. Studies have shown that when the pH of gastric juice is <3, Klebsiella pneumoniae rarely exists. According to de Frock et al., it was confirmed that under pathological conditions, the new gram-negative bacilli colonies in the pharynx are related to the bacteria previously found in the feces. Moreover, as the bacterial colonies in the feces change during hospitalization, the pharyngeal bacterial colonies will also change accordingly. After McAedingham performed selective decontamination of the digestive tract, he found that the respiratory tract infection rate in the disinfection group was six times lower than that in the control group, and the bacterial colonies in the pharynx and rectum were also significantly reduced.

In order to prevent stress ulcers in severe patients, the use of antacids and/or H2 receptor antagonists can lead to an increase in pharyngeal bacterial colony colonization and an increase in respiratory infections, which has been confirmed by many clinical studies. 9.3 The lung’s own defense mechanism

When Klebsiella pneumoniae enters the alveoli, the lung’s own defense phagocytosis system first carries out self-defense to prevent infection. In the alveoli, polymorphonuclear granulocytes (PMN) are mainly responsible for the resistance to Klebsiella pneumoniae. Rehm et al.'s study showed that neutrophil-deficient mice can quickly clear Staphylococcus aureus in the alveoli, but cannot clear Klebsiella pneumoniae. Studies have shown that the tiny capsule of Klebsiella pneumoniae prevents phagocytes from entering the central area of ??infection. From animal models of Klebsiella pneumoniae pneumonia, it can be found that the main reason for the strong pathogenicity of thick-capsulated strains is that they are resistant to phagocytosis in animals. When bacteria invade the alveoli, the alveolar cavities are filled with a large number of neutrophils. The process of PMN phagocytosis of Klebsiella pneumoniae in the alveolar cavities can be observed through a microscope. This is due to the bacterial activation of various lymphoid chemotactic factors in the lungs. *, chemokines are released into the alveoli, inducing PMN to continuously replenish the alveolar space from the circulation. The chemotactic component is mainly complement within 4 to 6 hours after the reaction begins, and the next 12 to 24 hours is the effect of non-complement chemokines. 9.4 Pathogenesis

Intratracheal inhalation (aspiration) is the key to the pathogenesis of pneumonia. 70 Aspiration can occur in normal people while sleeping, but whether aspiration causes illness depends on the amount of bacteria inhaled in the pharynx reaching a certain concentration. Recent studies have shown that gram-negative bacilli colonies in the pharynx are an autonomous defense function of the respiratory tract in critically ill patients. One sign of the deficiency is that once the bacteria are inhaled into the lower respiratory tract, pneumonia can develop. In addition, in addition to the dense bacterial colonies in the pharynx, the following factors can also increase airway aspiration: ① Confusion or coma. ②Abnormal sphincter function reflex. ③Delayed gastric emptying and weakened activity. ④ Swallowing dysfunction. ⑤Leakage of bacteria around the tracheal intubation cuff, etc. The specific pathogenesis is shown in Figure 1: 9.5 Pathological changes

Primary Klebsiella pneumoniae pneumonia is mostly distributed in large lobes and is common in the upper lobes of the lungs, especially the right upper lobe; secondary pneumonia is more common It is distributed in lobules, showing symptoms like patchy bronchopneumonia in both lungs. Multiple lobes, bilaterality and lobular distribution are rare. The overall pathology is similar to pneumococcal pneumonia, but it develops faster. There are no obvious stage changes of pneumonia, but there are Its own characteristics: ① In the autopsy of the diseased lung lobes, mucus-like exudate can be seen flowing out of the cut section, or thick filamentous exudate can be stirred up, which is a characteristic change of its pathology. ② Lung tissue is destroyed rapidly, and multiple abscesses or a single large abscess can form within 4 days. The alveolar walls are destroyed, causing alveolar atrophy and lung volume reduction. Main pulmonary blood vessels can be embolized, causing secondary pulmonary gangrene and necrosis. ③ It is often combined with pleural invasion, pleural fibrinous exudation, and adhesion, with an incidence rate of about 25%, and may even be combined with pericardial effusion. ④ In the early histological examination, edema fluid, monocytes and bacteria can be seen. In the later stage, alveolar wall destruction, a large number of polymorphonuclear neutrophils, active fibrous tissue proliferation, and easy organic changes can be seen. ⑤ It can cause pulmonary hemorrhage, pyopneumothorax, pericarditis, bronchiectasis and other changes, and some may become chronic Klebsiella pneumonia. 10 Clinical manifestations of Klebsiella pneumoniae pneumonia 10.1 Symptoms

Klebsiella pneumoniae pneumonia has a sudden onset, characterized by chills, high fever, cough, purulent sputum, and brick-red jelly sputum. 80% of patients have chest pain, which is mainly caused by inflammation that invades the parietal pleura. Some patients have gastrointestinal symptoms, such as nausea, vomiting, diarrhea, jaundice, etc. The whole body is weak, and some patients have symptoms of upper respiratory tract infection. A very small number of patients present with a chronic disease course, which may also be delayed from an acute disease course. Symptoms include low-grade fever, cough, and weight loss. 10.2 Signs

Acute illness, dyspnea, cyanosis, and a few patients may develop jaundice and shock. Wet rales can be heard in the lungs. White blood cells and neutrophils were increased, and sputum culture was positive.

11 Complications of Klebsiella pneumoniae pneumonia

Complications of Klebsiella pneumoniae pneumonia include empyema, pneumothorax, pericarditis, meningitis and polyarthritis. 12 Laboratory tests 12.1 Blood tests

Most patients have increased white blood cells, with an average range of (150-200) × 109/L. Among them, there are toxic particles and left-shifted nuclei, about 1/4 of the patients The total number of white blood cells is normal or reduced. Leukopenia is often a sign of poor prognosis, and patients are often accompanied by anemia. 12.2 Sputum or bronchial aspirate smear and/or culture

The detection of Klebsiella pneumoniae is the basis for diagnosis, but it is affected by many factors.

(1) Under pathological conditions, the colonization rate of Klebsiella pneumoniae in the pharynx is very high, and it is easy to cause specimen contamination in the oropharynx.

(2) Single Klebsiella pneumoniae pneumonia is decreasing, while mixed infections with multiple bacteria are increasing (especially nosocomial infections). It is often impossible to determine the main bacterial agent.

At present, scholars at home and abroad believe that the sensitivity, specificity and reliability of sputum examination are not ideal. Many patients do not have much sputum, and even if there is sputum, sometimes no bacteria can be found. Although some patients can pass Culture confirms, but is of little help in initial diagnosis and treatment. However, according to the current situation and conditions of various hospitals in my country, sputum smear Gram staining and culture are still an important preliminary screening method and diagnostic measure. 13 Auxiliary examination

X-ray findings: lobar consolidation, lobular infiltration, and abscess formation. Large leaf consolidations are mostly located in the right upper lobe. Due to the large amount of inflammatory exudate, which is thick and heavy, the interleaf fissures fall in an arc shape. Abscesses, pleural effusion, and rarely bronchopneumonia are seen in inflammatory infiltrates. 14 Diagnosis of Klebsiella pneumoniae pneumonia

Middle-aged and elderly men, long-term alcoholics, chronic bronchitis or other lung diseases, diabetes, malignant tumors, organ transplantation, or immunosuppression such as granulocytopenia, Or when patients with artificial airway mechanical ventilation develop fever, cough, sputum production, dyspnea, moist rales in the lungs, increased blood neutrophils, and pulmonary inflammatory infiltrates on X-ray, suggesting bacterial pneumonia. , the possibility of pneumonia caused by Clostridium pneumoniae should be considered, especially when treatment with penicillin or erythromycin and other macrolide antibiotics is ineffective. The clinical manifestations, laboratory and X-ray examination of B. pneumoniae pneumonia are mostly non-specific. Although coughing up brick-red sputum is a typical symptom, it is rare clinically. Microbiological examination is the only basis for diagnosing pneumonia caused by B. pneumoniae, and it is also an important method for distinguishing it from other bacterial pneumonias.

More gram-negative bacilli are found in smears of qualified sputum specimens, especially those that gather in large numbers around pus cells and pseudostratified ciliated columnar epithelial cells of the bronchus and have capsules, so pneumoniae bacilli should be considered. Pneumonia is a possibility, but it is not the basis for diagnosis. Isolation of K. pneumoniae by sputum culture is helpful for diagnosis, but it should be distinguished from contaminating bacteria colonizing the oropharynx. If B. pneumoniae is isolated from sputum samples screened by smears for more than two consecutive times or the concentration of B. pneumoniae isolated by quantitative sputum culture is >106CFU/ml or the semi-quantitative concentration is ? or , it can be diagnosed as B. pneumoniae pneumonia. For severe, refractory or immunosuppressed cases, anti-contamination lower respiratory tract specimen sampling techniques such as transcricothyroid tracheal aspiration (TTA), anti-contamination double cannula brush sampling (PSB), bronchoalveolar lavage (BAL) and Percutaneous lung aspiration (LA), etc., the disease can be diagnosed by isolating pneumoniae bacilli from these specimens. It is necessary to pay attention to and actively carry out bacterial culture of blood or pleural fluid. If it is positive, it is not only of diagnostic significance, but also very important for selecting sensitive antibacterial drugs and improving prognosis.

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Medical encyclopedia, calculate now! 15 Differential diagnosis

It should be clinically differentiated from acute caseous pneumonia, bronchiectasis, Streptococcus pneumoniae pneumonia, etc. 16 Treatment of Klebsiella pneumoniae pneumonia

Treatment of Klebsiella pneumoniae pneumonia includes anti-infective treatment and supportive care. Whether anti-infective treatment is effective or not directly affects the prognosis of the disease. Before the era of antibiotics, the mortality rate of pneumonia due to B. pneumoniae was as high as 51 to 97. Under antibiotic treatment, the case fatality rate has dropped significantly, but due to the high drug resistance rate of pneumoniae bacteria, the case fatality rate is 20 to 30, which is still higher than that of Streptococcus pneumoniae pneumonia.

There are many drugs with antibacterial activity against pneumoniae, including first to fourth generation cephalosporins, broad-spectrum penicillins, aminoglycoside antibiotics, fluoroquinolones, carbapenems and monocyclic β Lactams, etc. Chloramphenicol and tetracycline have antibacterial effects, but there are many drug-resistant strains and few clinical applications. High efficiency, low toxicity and low price are the most important factors when considering the selection of antibacterial drugs. With the expansion of clinically available drug varieties and the increasing number of multi-drug-resistant strains, reasonable selection should be based on drug susceptibility testing. Before the results of drug susceptibility testing are obtained, or the unit has not conducted drug susceptibility testing, or when several antibacterial drugs tested show resistance, empirical medication is the only option for formulating an anti-infection plan. Empirical drug use should emphasize the selection of drugs based on previous bacterial resistance monitoring results in the region, unit, and even department.

It is usually recommended to use second, third or fourth generation cephalosporins or combined with aminoglycosides. If there are drug susceptibility results, cephalosporins alone can also be used. Commonly used methods: intravenous infusion of cefotaxime 2g once every 8 hours or intravenous infusion of ceftriaxone 2g once a day. Aztreonam and second-generation cephalosporins such as cefuroxime can also be used. In areas where the frequency of antibiotic use is low and drug resistance is not serious, especially for community infections with mild illness, first-generation cephalosporins such as cefazolin and cefradine can be used at a dose of 4 to 6 g/d, divided into 2 to 4 intravenous infusions. Among penicillins, the resistance rate to ampicillin is already very high, but the new generation of broad-spectrum penicillins such as piperacillin have better therapeutic effects on pneumonia caused by Clostridium pneumoniae.

Aminoglycosides include gentamicin, but there are many resistant strains. Nowadays, amikacin is commonly used, and the usual dosage is 0.4-0.6g/d, intravenously infused in 1-2 times. Since aminoglycosides cannot easily penetrate bronchial mucosa and sputum, the concentration of antibiotics in bronchial secretions is only 5 to 40 times the blood concentration, and the acidic environment of sputum will significantly reduce the antibacterial activity of antibiotics. Therefore, the clinical use of aminoglycosides is The efficacy is often inferior to in vitro drug sensitivity testing. Therefore, for pulmonary infections, especially severe infections, aminoglycosides should be used in combination with β-lactams rather than used alone.

Fluoroquinolones such as ciprofloxacin, levofloxacin, levofloxacin, etc., cephalomycin such as cefoxitin, cefmetazole, β-lactams/β-lactamase Inhibitor combinations such as sutacillin (ampicillin/sulbactam), cefoperazone/sulbactam/sulbactam, piperacillin/clavulanic acid, etc., include many drug-resistant strains of pneumoniae and also have Good antibacterial activity, worth choosing.

In recent years, the detection rate of extended-spectrum beta-lactamase (ESBL)-producing strains of Bacillus pneumoniae has increased significantly in some areas, especially in nosocomial pneumonia. In many ICU infection strains, ESBL accounts for 10% of pneumoniae strains. 20～30. For infections caused by such strains, carbapenems such as imipenem, meropenem, etc. are the first choice. Medication method: imipenem 0.5g intravenous infusion, once every 8 hours, or 1 g intravenous infusion , once every 12 hours.

Cefoperazone/sulba/sulbactam also has good antibacterial activity against ESBL strains of K. pneumoniae.

The course of anti-infective treatment for B. pneumoniae pneumonia is generally 10 to 14 days. If the lesions are extensive, especially if there are multiple small abscesses, the course will be at least 3 weeks. Supportive treatment includes keeping the airway open, giving oxygen, correcting water, electrolyte and acid balance imbalances, supplementing nutrition, etc., which cannot be ignored in the treatment of pneumonia caused by Clostridium pneumoniae. 17 Prognosis

The prognosis of patients with positive blood cultures is generally poor. Due to the high drug resistance rate of pneumonia bacteria, the case fatality rate is 20 to 30. 18 Prevention of Klebsiella pneumoniae pneumonia 18.1 Strictly implement the disinfection and isolation system

This is mainly for medical staff and the hospital environment and equipment. Strictly wash hands and wear gloves before and after contact with patients. Regular environmental and Indoor disinfection and ventilation, regular cleaning and disinfection of respiratory treatment devices as required, regular replacement of mechanical ventilation and atomizer pipelines, etc., and a complete set of strict nosocomial infection monitoring and prevention plans. According to reports, hospitals that adopt this program have 20% lower nosocomial infection rates than those that do not. 18.2 Gastrointestinal decontamination treatment

Gastrointestinal decontamination treatment is a preventive measure commonly used in Europe in recent years. It is mainly targeted at people susceptible to nosocomial infections. The purpose is to remove bacterial colonies in the gastrointestinal tract. Reproduction and growth. Methods include total gastrointestinal decontamination and selective gastrointestinal decontamination. The latter is commonly used. It uses nasal feeding or oral administration of polymyxin B, tobramycin (gentamicin or neomycin) that are not absorbed by the gastrointestinal tract. (mycin, etc.) and amphotericin B for 5 days, and systemic application of cephalosporins every day to remove aerobic bacteria from the oropharynx and gastrointestinal tract without reducing the number of anaerobic bacteria. Its preventive effect is on Gram This is especially obvious for negative bacilli. According to the author's statistics on relevant literature, there are almost no secondary pneumonia and respiratory infections caused by Klebsiella pneumoniae in the decontamination group (some are infections caused by drug-resistant strains). 18.3 Protect the acid barrier of the stomach

Sucralfate (ulcerlmin) is mainly used to prevent stress ulcers. It can not only prevent stress ulcer bleeding, but also has the ability to adsorb gastric mucosa. , change gastric mucus, increase prostaglandin E2 (PGE2) content in the gastric cavity, and absorb pepsin without changing the acidic environment in the stomach, thus effectively preventing ulcers and infection. And according to the literature, sulfur Sucralfate still has inherent bactericidal activity. A series of studies have shown that the incidence of pneumonia in the antacid group was 23 to 35, while the incidence of pneumonia in the sucralfate group was 10 to 19. 18.4 Biological prevention

Biological prevention methods for Klebsiella pneumoniae pneumonia are still in the experimental stage. Held et al. injected IgM monoclonal antibodies (MAb) induced from Klebsiella pneumoniae capsular polysaccharide (CPS) into experimental animals to prevent Klebsiella pneumoniae pneumonia. Compared with the control group, regardless of the organ involvement rate and infected tissue, Held et al. In terms of the number of bacteria and histological changes in the lungs, the prevention group was far better than the control group (P<0.01). However, this MAb has no effect in preventing Klebsiella pneumoniae from entering the lungs, but accelerates the absorption of infection. Enhance the lung's ability to eliminate bacteria. There are also some similar experimental reports, but mature vaccines and antibodies have not yet been used in clinical applications and require further research.

Klebsiella pneumoniae pneumonia has harmed humans for more than a century. With the development of science, the continuous improvement of examination and treatment methods, and the gradual deepening of human understanding of it, it is believed that its incidence can be further reduced. and case fatality rate to achieve greater progress.

19 Related drugs

Oxygen, cyclosporine, penicillin, erythromycin, chloramphenicol, tetracycline, cefotaxime, ceftriaxone, aztreonam, cefuroxime, cefazolin, cefradine, Ampicillin, piperacillin, gentamicin, amikacin, ciprofloxacin, levofloxacin, ofloxacin, cefoxitin, cefmetazole, sutacillin, cefoperazone, cefoperazone/sultamide Bactam, clavulanic acid, imipenem, meropenem, polymyxin, tobramycin, neomycin, sucralfate, pepsin 20 related tests

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